Search results
Results from the WOW.Com Content Network
Wallerian degeneration occurs after axonal injury in both the peripheral nervous system (PNS) and central nervous system (CNS). It occurs in the section of the axon distal to the site of injury and usually begins within 24–36 hours of a lesion. Prior to degeneration, the distal section of the axon tends to remain electrically excitable.
Diffuse axonal injury after a motorcycle accident. MRI after 3 days: on T1-weighted images the injury is barely visible. On the FLAIR, DWI and T2*-weighted images a small bleed is identifiable. DAI is difficult to detect since it does not show up well on CT scans or with other macroscopic imaging techniques, though it shows up microscopically. [9]
Slower degeneration of the distal segment than that which occurs in the peripheral nervous system also contributes to the inhibitory environment because inhibitory myelin and axonal debris are not cleared away as quickly. All these factors contribute to the formation of what is known as a glial scar, which axons cannot grow across. [9]
Neurapraxia is a temporary interruption of conduction without loss of axonal continuity. [3] Neurapraxia involves a physiologic block of nerve conduction in the affected axons. Other characteristics: mildest type of nerve injury; sensory-motor problems present distal to the site of injury; intact endoneurium, perineurium, and the epineurium
Axonal transport can be disrupted by a variety of mechanisms including damage to: kinesin and cytoplasmic dynein, microtubules, cargoes, and mitochondria. [25] When axonal transport is severely disrupted a degenerative pathway known as Wallerian-like degeneration is often triggered. [71]
Such lesions give rise to extensive astrocyte loss, which may occur in part in the absence of any other tissue injury, such as demyelination or axonal degeneration (lesion type 5). Finally, lesions with a variable degree of astrocyte clasmatodendrosis are found, which show plaque-like primary demyelination that is associated with ...
CMT2 variants are typically referred to as axonal neuropathies due to the axonal degeneration observed. CMT2 variants are a result of damage to the nerve axons, rather than damage to the myelin sheath (as is the case with CMT1). Damaged axons cause slowed transmission of signals to the muscles and brain, causing symptoms including muscle ...
Motor and sensory functions distal to the point of injury are completely lost over time leading to Wallerian degeneration due to ischemia, or loss of blood supply. Axonotmesis is usually the result of a more severe crush or contusion than neurapraxia. [1] Axonotmesis mainly follows a stretch injury.